Acute Decompensated Heart Failure

📋 Key Information Summary

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Acute decompensated heart failure (ADHF) presents with dyspnoea, fluid overload, and/or hypoperfusion and accounts for over 60,000 hospitalisations annually in Australia.
Classify patients using the Nohria–Stevenson haemodynamic profile: warm–dry (compensated), warm–wet (congestion only), cold–dry (hypoperfusion), cold–wet (congestion + hypoperfusion) — this drives initial therapy.
BNP ≥ 100 pg/mL or NT-proBNP ≥ 300 pg/mL supports diagnosis; serial measurement aids prognostication but must be interpreted in clinical context (obesity, AF, renal impairment alter thresholds).
IV furosemide is first-line diuretic therapy; administer at ≥ the patient's home oral dose (or 1 mg IV ≈ 2 mg PO furosemide), given as bolus or continuous infusion, reassessing diuretic response at 2 hours via urine output.
Diuretic resistance (inadequate diuresis despite high-dose loop diuretics) should prompt sequential nephron blockade with metolazone or thiazide, or consideration of ultrafiltration in refractory cases.
IV glyceryl trinitrate (GTN) is the primary vasodilator for ADHF with hypertension and pulmonary oedema; start at 10–20 mcg/min and titrate to SBP target; avoid in severe aortic stenosis or SBP < 90 mmHg.
Inotropic agents (dobutamine, milrinone, levosimendan) are reserved for cardiogenic shock or severe hypoperfusion; they increase mortality risk with routine use and should be weaned as soon as clinically feasible.
Decongestion endpoints include weight loss ≥ 0.5–1.0 kg/day, net fluid loss ≥ 1–1.5 L/day, resolution of orthopnoea, JVP < 8 cm, and absence of peripheral oedema — aim for euvolaemia before discharge.
Optimise guideline-directed medical therapy (GDMT) before discharge: ACEi/ARB/ARNI, beta-blocker, MRA, SGLT2 inhibitor — initiate or uptitrate during admission where tolerated.
Early follow-up within 7 days of discharge is critical; multidisciplinary heart failure programs reduce 30-day readmission rates by 25–35% and are recommended by the Australian Clinical Standards for Heart Failure.
Aboriginal and Torres Strait Islander Australians have 2–3× the heart failure hospitalisation rate; culturally responsive care, remote access pathways, and cardiac rehabilitation programmes are essential to reduce disparities.
SGLT2 inhibitors (dapagliflozin, empagliflozin) are now a foundational pillar of HF therapy regardless of diabetes status; initiate in-hospital once euvolaemic and haemodynamically stable.

Introduction & Australian Epidemiology

Acute decompensated heart failure (ADHF) is a clinical syndrome characterised by the rapid onset or worsening of symptoms and signs of heart failure requiring urgent medical attention and often hospitalisation. It encompasses a heterogeneous group of presentations ranging from acute pulmonary oedema to cardiogenic shock, and may occur in patients with previously diagnosed chronic heart failure (HF) or as the de novo manifestation of cardiac disease.

In Australia, heart failure affects an estimated 480,000 individuals, with prevalence rising sharply with age — affecting up to 10–15% of Australians aged ≥ 75 years. The Australian Institute of Health and Welfare (AIHW) reports approximately 62,000 hospitalisations per year with a principal diagnosis of heart failure, making it one of the leading causes of acute medical admission. In-hospital mortality ranges from 4–8%, with 30-day readmission rates of 20–30%, representing a significant burden on the Australian healthcare system estimated at over $2.7 billion annually.

Approximately half of all HF hospitalisations in Australia involve heart failure with reduced ejection fraction (HFrEF, LVEF ≤ 40%), while heart failure with preserved ejection fraction (HFpEF, LVEF ≥ 50%) accounts for a growing proportion, particularly in older, female, and hypertensive populations. Heart failure with mildly reduced ejection fraction (HFmrEF, LVEF 41–49%) is increasingly recognised as a distinct entity.

The Australian Clinical Standards for Heart Failure (ACSQHC, 2021) and the National Heart Foundation of Australia / Cardiac Society of Australia and New Zealand (CSANZ) guidelines provide the framework for evidence-based management. This article focuses on the acute in-hospital management of ADHF, with emphasis on classification, pharmacotherapy, and the transition to optimal outpatient care.

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Burden of disease: Heart failure readmissions are a key quality indicator under the National Health Reform Agreement. Australian hospitals participating in the Heart Failure Clinical Quality Registry have demonstrated that structured discharge programmes significantly reduce preventable readmissions.

Initial Assessment & Classification

Clinical Presentation

Patients with ADHF typically present with one or more of the following: acute dyspnoea at rest or with minimal exertion, orthopnoea, paroxysmal nocturnal dyspnoea, peripheral oedema, weight gain over days, fatigue, and exercise intolerance. Physical examination findings include elevated jugular venous pressure (JVP), bibasilar crackles, S3 gallop, peripheral oedema, hepatomegaly, and cool extremities (in low-output states).

Haemodynamic Classification — The Nohria–Stevenson Profiles

The cornerstone of initial ADHF assessment is the rapid haemodynamic classification using the Nohria–Stevenson framework, which categorises patients along two axes: perfusion (warm vs cold) and volume status (wet vs dry).

Profile A

Warm & Dry (Compensated)

Adequate perfusion, euvolaemic. No congestion, no hypoperfusion. SBP > 90 mmHg, no peripheral oedema, warm extremities, clear lungs.

Setting: Outpatient optimisation, rarely presents acutely

Profile B

Warm & Wet (Congested)

Adequate perfusion with signs of congestion. Most common ADHF presentation (≈75%). Elevated JVP, crackles, peripheral oedema, weight gain. SBP usually maintained.

Setting: Ward-based care, diuretics ± vasodilators

Profile C

Cold & Wet (Congestion + Hypoperfusion)

Congestion with signs of hypoperfusion: cool peripheries, narrow pulse pressure, altered mentation, rising creatinine, hepatomegaly, lactate > 2 mmol/L.

Setting: HDU/ICU, inotropes + diuretics ± vasopressors

Profile L

Cold & Dry (Hypoperfusion)

Hypoperfusion without congestion — often post-diuresis or in advanced low-output HF. Narrow pulse pressure, low SBP, prerenal azotaemia, fatigue.

Setting: ICU, inotropes ± mechanical circulatory support assessment

Clinical Assessment Priorities

History: Prior HF diagnosis, LVEF, current medications, dietary indiscretion, medication non-adherence, recent intercurrent illness (AF, ACS, PE, infection, anaemia).
Examination: JVP, lung crackles, S3/S4, peripheral oedema grade, capillary refill time, urine output (insert catheter if oliguric or shock), hepatomegaly, ascites.
Vital signs: HR, BP (arm + leg if coarctation suspected), SpO₂, RR, temperature, weight (if recent baseline available).

BNP and NT-proBNP

Natriuretic peptides are essential in confirming the diagnosis and assessing severity. BNP and NT-proBNP are available through all Australian public hospital pathology services and most community laboratories (MBS item 66546 — BNP; MBS item 66551 — NT-proBNP).

Biomarker	Exclusion Threshold	Grey Zone	Likely ADHF
BNP	< 100 pg/mL	100–400 pg/mL	> 400 pg/mL
NT-proBNP	< 300 pg/mL	300–2000 pg/mL (age-dependent)	> 2000 pg/mL (≥ 75 yrs: > 450; 50–75 yrs: > 900)

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Interpreting natriuretic peptides: BNP may be falsely low in obesity (high adipose tissue clearance), flash pulmonary oedema (insufficient time for rise), and in some HFpEF presentations. NT-proBNP is affected by renal impairment (eGFR < 60) — use age-adjusted cut-offs. AF elevates both BNP and NT-proBNP independently of HF. Always interpret alongside clinical assessment.

Essential Initial Investigations

Essential

ECG (12-lead)

Rhythm (AF common trigger), ischaemic changes (ST/T), LVH, QRS duration (CRT candidacy), conduction abnormalities.

Essential

Chest X-ray

Pulmonary congestion, pleural effusion, cardiomegaly, pulmonary oedema (upper lobe diversion, Kerley B lines, peribatcuffing). Rule out pneumonia, pneumothorax.

Essential

Bloods — FBC, UEC, LFTs, TFTs, glucose, lipid, iron studies, HbA1c

Renal function (baseline + trajectory), hepatic congestion, anaemia (contributor), thyroid disease (reversible cause), iron deficiency (ferritin < 100 or 100–299 with TSAT < 20%).

Available

Troponin (high-sensitivity)

Elevated in ADHF from myocardial strain; rule out acute coronary syndrome as precipitant. Differentiate using clinical context and serial trending.

Available

Venous blood gas / lactate

Lactate > 2 mmol/L suggests hypoperfusion (cold profile); metabolic acidosis severity guides inotrope need. VBG for potassium (urgent if diuretic-related).

Specialist

Transthoracic echocardiography

Urgent if new diagnosis, haemodynamic instability, suspected mechanical complication (VSD, papillary muscle rupture), or valvular emergency. Assess LVEF, wall motion, diastolic function, RV function, valvular disease, pericardial effusion.

Diuretic Strategies

Intravenous loop diuretics are the mainstay of decongestion therapy in ADHF. The goal is to achieve effective diuresis — defined as a net fluid loss of 1–1.5 litres per day and weight loss of 0.5–1.0 kg/day — with attention to renal function and electrolyte balance.

First-Line: IV Furosemide

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Furosemide

Lasix®, Urex® · Loop diuretic

Adult dose Initial: ≥ home oral dose IV (or 1:2 conversion, e.g. 40 mg PO → 20 mg IV) given as IV bolus. Typical starting dose 20–80 mg IV bolus. Escalate to 2.5× home dose if no response in 2 hours (urine output < 100–150 mL/hr).

Continuous infusion 5–20 mg/hr IV after loading bolus — may be superior to bolus dosing in severe congestion (diuresis of 3.5 L/day target). Requires urinary catheter and hourly output monitoring.

Renal adjustment Higher doses needed with eGFR < 30 (bioavailability of oral form drops); up to 250–500 mg IV bolus in resistant cases under nephrology guidance.

PBS status ✔ PBS General Benefit

Alternative: Bumetanide

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Bumetanide

Burinex® · Loop diuretic

Adult dose 1–2 mg IV bolus, repeat 2-hourly PRN. Approximately 40× more potent than furosemide (1 mg bumetanide ≈ 40 mg furosemide). Better oral bioavailability in severe oedema (80% vs 10–100% for furosemide).

Renal adjustment Less affected by renal impairment than furosemide. Useful when furosemide response is suboptimal.

PBS status ✔ PBS General Benefit

The "2-Hour Rule" — Assessing Diuretic Response

After each IV diuretic dose, urine output should be measured over 2 hours (indwelling catheter recommended for all inpatients receiving IV diuretics). The response guides escalation:

2-Hour Urine Output	Response	Action
> 200 mL (furosemide) / > 60 mL (bumetanide)	Good response	Repeat same dose at 4–6 hourly intervals or convert to continuous infusion
100–200 mL (furosemide) / 30–60 mL (bumetanide)	Partial response	Double the diuretic dose; reassess at 2 hours
< 100 mL (furosemide) / < 30 mL (bumetanide)	Poor response (diuretic resistance)	Add sequential nephron blockade (metolazone) or switch strategy; consider ultrafiltration

Diuretic Resistance

Diuretic resistance is defined as failure to achieve adequate diuresis despite escalating doses of IV loop diuretics. Causes include: inadequate dose, poor gut absorption (in severe oedema), excessive sodium intake, NSAID use, severe renal impairment, nephrotic syndrome, and neurohormonal activation causing sodium avidity.

1

Confirm adherence and dose adequacy

Ensure the patient has received adequate IV doses; consider continuous infusion. Exclude NSAIDs, excessive dietary sodium (> 2 g/day), or interacting medications.

2

Sequential nephron blockade

Add metolazone 2.5–5 mg PO (given 30 min before loop diuretic) or IV chlorothiazide 500 mg–1 g if metolazone unavailable. This exploits the "sequential blockade" — thiazides block the distal tubule compensatory reabsorption.

3

Consider IV vasodilator

If SBP permits (> 100 mmHg), IV GTN reduces preload and afterload, augmenting diuretic efficacy.

4

Ultrafiltration

If resistance persists after 48–72 hours of aggressive combination diuresis, refer for mechanical fluid removal. Indicated for refractory volume overload with congestion despite maximal pharmacotherapy.

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Metolazone

Zaroxolyn® · Thiazide-like diuretic

Adult dose 2.5–5 mg PO once daily, given 30 min before loop diuretic. Can be used on consecutive days but monitor closely for excessive diuresis and electrolyte derangement.

Renal adjustment Effective even with eGFR < 30 (unlike thiazides). Use with caution — risk of severe hypokalaemia and hyponatraemia when combined with loop diuretics.

PBS status ⚠ PBS Authority Required

Ultrafiltration

Peripheral ultrafiltration (UF) involves extracorporeal removal of isotonic fluid via a central venous catheter or large-bore peripheral IV. The AVOID-HF and CARRESS-HF trials have provided mixed evidence; UF is generally reserved for patients with refractory congestion unresponsive to combination diuretic therapy, particularly when renal function is deteriorating ("cardiorenal syndrome"). Australian centres with HF specialist services (e.g., major tertiary hospitals) offer UF; referral to a HF cardiologist is required. Rate of fluid removal is typically 200–500 mL/hr, tailored to haemodynamic tolerance.

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Monitoring during diuresis: Check UEC at least daily during active diuresis. Watch for hypokalaemia (K⁺ < 3.5 mmol/L — supplement with IV/PO KCl), hyponatraemia (Na⁺ < 130 mmol/L — fluid restrict, consider tolvaptan in euvolaemic hyponatraemia), hypomagnesaemia, and prerenal AKI (rising creatinine without congestion — may need to reduce diuretic dose). Always replace potassium and magnesium aggressively.

Vasodilator Therapy

Vasodilators are indicated in ADHF with congestion and adequate or elevated blood pressure (warm–wet profile, typically SBP > 110 mmHg). They reduce preload (venodilation) and afterload (arteriolar dilation), rapidly improving symptoms of pulmonary oedema. The choice of vasodilator depends on severity, blood pressure, and local availability.

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Glyceryl Trinitrate (GTN)

Anginine®, Nitrolingual® · Nitrate vasodilator

Indication First-line vasodilator for ADHF with pulmonary oedema and SBP > 110 mmHg. Rapid onset, titratable.

Adult dose IV infusion: start 10–20 mcg/min, titrate by 10–20 mcg/min every 5 min to symptom relief (max 200 mcg/min typically; higher doses may be needed). Target: SBP reduction of 20–30% or symptomatic improvement.

Monitoring Continuous arterial BP monitoring (arterial line if haemodynamically compromised) or NIBP q5min during titration. HR, SpO₂, headache (common, dose-limiting). Avoid if SBP < 90 mmHg or recent PDE5 inhibitor use (sildenafil within 24 hrs, tadalafil within 48 hrs).

Contraindications Severe aortic stenosis, hypertrophic obstructive cardiomyopathy (HOCM), RV infarction, constrictive pericarditis, concurrent PDE5 inhibitor use.

PBS status ✔ PBS General Benefit

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Sodium Nitroprusside

Nipride® · Balanced arterial + venous vasodilator

Indication Severe ADHF with hypertension and significant afterload excess (e.g. acute aortic regurgitation, hypertensive emergency with HF). More potent afterload reducer than GTN.

Adult dose IV infusion: start 0.3 mcg/kg/min, titrate by 0.5 mcg/kg/min every 5 min. Usual range 0.5–5 mcg/kg/min. Max 10 mcg/kg/min for no more than 72 hours.

Monitoring Intra-arterial BP line mandatory. Thiocyanate levels if infusion > 48 hrs or renal/hepatic impairment (toxicity risk: confusion, seizures). Protect from light (wrap tubing). Cyanide toxicity risk — co-administer sodium thiosulfate if prolonged use.

Availability Available in Australian ICUs and cardiac catheterisation labs. Not routinely stocked on general wards. Requires ICU/HDU monitoring.

PBS status ⚠ Not PBS-listed for this indication (hospital supply)

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Nesiritide (BNP analogue)

Natrecor® · Recombinant human BNP

Indication ADHF with dyspnoea at rest. Provides venous and arterial vasodilation with modest diuretic effect. ASCEND-HF trial showed symptom relief without mortality benefit.

Adult dose IV bolus: 2 mcg/kg (optional — many centres omit the bolus to reduce hypotension), then infusion 0.01 mcg/kg/min. May increase to 0.03 mcg/kg/min. Duration: 24–72 hours typically.

Monitoring BP q15min during initiation. Avoid if SBP < 90 mmHg. Caution with concurrent ACEi/ARB (hypotension risk). Renal function — may worsen GFR at higher doses.

Availability Limited availability in Australia. Not widely used. Obtain through hospital pharmacy special access scheme.

PBS status ✘ Not PBS-listed

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Vasodilator safety: All IV vasodilators risk precipitous hypotension. SBP < 90 mmHg is an absolute contraindication for initiation. When using nitrates, check for concomitant PDE5 inhibitor use (sildenafil, tadalafil, vardenafil) — combined use causes life-threatening hypotension. In patients with RV failure (inferior STEMI), nitrates may cause profound preload-dependent hypotension — use extreme caution or avoid.

Vasodilator Selection Guide

Scenario	Preferred Agent	Rationale
Acute pulmonary oedema, SBP > 140	IV GTN	Rapid onset, titratable, widely available
Hypertensive HF emergency	IV Nitroprusside or GTN (high dose)	Potent afterload reduction; requires arterial line
Warm–wet, SBP 100–140	IV GTN (conservative titration) ± diuretic	Titrate cautiously; monitor BP closely
ADHF with RV predominant failure	Avoid GTN; consider nitroprusside if afterload excess	RV preload-dependent; nitrates can precipitate cardiovascular collapse

Inotropic Support

Inotropic agents are reserved for ADHF with evidence of hypoperfusion (cold profiles — Nohria–Stevenson C or L) manifesting as: hypotension (SBP < 90 mmHg or MAP < 65 mmHg), signs of end-organ hypoperfusion (oliguria, altered mentation, rising lactate, cool extremities), and cardiogenic shock. These agents carry significant risk — including arrhythmia, myocardial ischaemia, and increased mortality — and should be used at the lowest effective dose for the shortest possible duration.

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Safety warning: Routine use of inotropes in ADHF without evidence of hypoperfusion (i.e. warm–wet profile) is associated with increased mortality (ADHERE registry, OPTIME-CHF trial). Inotropes should NOT be used as diuretic adjuncts in the absence of haemodynamic compromise. Always have a clear haemodynamic endpoint and weaning plan before initiating.

Indications for Inotropic Support

Cardiogenic shock (SBP < 90 mmHg + signs of hypoperfusion + raised filling pressures)
Low-output syndrome post-cardiac surgery or acute myocardial infarction
Bridge to decision / bridge to advanced therapies (transplant, LVAD)
Acute decompensation of severe chronic HF (LVEF < 25%) with end-organ dysfunction despite optimal diuretic and vasodilator therapy
Right ventricular failure with haemodynamic compromise

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Dobutamine

Dobutrex® · β1-agonist inotrope

Mechanism Predominantly β1-agonist with modest β2-vasodilatory effects. Increases cardiac contractility and output with mild reduction in SVR. Net effect: increased CO, reduced filling pressures.

Adult dose 2.5–20 mcg/kg/min IV infusion. Start at 2.5–5 mcg/kg/min and titrate to effect (target CI > 2.2 L/min/m² or clinical improvement). Usual effective range 5–10 mcg/kg/min.

Monitoring Continuous ECG, arterial BP (intra-arterial line), CVP/PAC if available. HR (tachycardia dose-limiting), arrhythmias (VT/VF risk), lactate trending, urine output, peripheral perfusion.

Weaning Wean by 2 mcg/kg/min increments every 6–12 hours as tolerated. Monitor for recurrent hypoperfusion during wean. Patients on dobutamine > 72 hrs may develop tachyphylaxis (β-receptor downregulation).

Key adverse effects Sinus tachycardia, AF, VT/VF, hypokalaemia, myocardial ischaemia (increased MVO₂). Avoid in HOCM (dynamic outflow obstruction).

PBS status ⚠ Hospital use only (not PBS-listed)

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Milrinone

Primacor® · PDE-III inhibitor (inodilator)

Mechanism Phosphodiesterase-III inhibitor — increases cAMP in cardiac myocytes (positive inotropy) and vascular smooth muscle (vasodilation). "Inodilator" — increases CO while reducing SVR and PVR.

Adult dose Loading dose: 50 mcg/kg IV over 10 min (often omitted in practice due to hypotension risk). Maintenance: 0.375–0.75 mcg/kg/min IV infusion. Reduce dose by 50% if eGFR < 30.

Renal adjustment Milrinone is renally excreted — reduce infusion rate by 50% for eGFR < 30 mL/min. Half-life extends from 1.5 hrs to 3–6 hrs in renal impairment.

Key advantages Particularly useful in RV failure (reduces PVR), beta-blocked patients (mechanism is β-receptor independent), and bridge to LVAD/transplant.

Key adverse effects Hypotension (more than dobutamine), arrhythmias (VT ~12%), thrombocytopaenia (rare). OPTIME-CHF: increased adverse events in non-cardiogenic shock ADHF.

PBS status ⚠ Hospital use only (not PBS-listed)

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Levosimendan

Simdax® · Calcium sensitiser + K-ATP opener

Mechanism Calcium sensitiser (increases myofilament Ca²⁺ sensitivity without increasing intracellular Ca²⁺), plus vasodilation via vascular K-ATP channel opening. Active metabolite (OR-1896) has a half-life of ~80 hrs — prolonged haemodynamic effect for 7–10 days after a single 24-hr infusion.

Adult dose Loading: 6–12 mcg/kg IV over 10 min (often omitted if SBP < 100 mmHg). Maintenance: 0.05–0.2 mcg/kg/min for 24 hours. The prolonged effect allows intermittent dosing (e.g. monthly infusions in advanced HF — LION-HEART trial).

Key advantages Unlike catecholamine inotropes, levosimendan does not increase myocardial oxygen demand and may have anti-stunning, anti-inflammatory, and anti-apoptotic properties. SURVIVE and REVIVE-II trials showed symptom improvement and BNP reduction. Potential mortality benefit when compared with dobutamine (meta-analyses).

Key adverse effects Hypotension (dose-dependent), headache, atrial fibrillation, hypokalaemia. Prolonged action limits rapid dose adjustment.

Availability in Australia TGA-registered but limited hospital formulary availability. Accessed through hospital pharmacy on a named-patient basis. Increasingly used in advanced HF centres for intermittent therapy in inotrope-dependent patients.

PBS status ✘ Not PBS-listed

Weaning Protocols

Weaning of inotropic support should begin as soon as clinical improvement permits. The approach varies by agent:

Dobutamine

Reduce by 2 mcg/kg/min every 6–12 hours if: SBP > 90 mmHg without vasopressor, urine output > 0.5 mL/kg/hr, lactate normalising, improving mentation. Monitor for recurrent hypotension at each reduction step. Discontinue when at 2.5 mcg/kg/min and clinically stable for 6 hrs.

Milrinone

Reduce by 0.125 mcg/kg/min every 6–12 hours. Extended half-life in renal impairment requires slower wean. Transition to oral milrinone (2.5–7.5 mg TDS) is possible for bridge to LVAD/transplant, though oral milrinone is not available in Australia — oral enoximone (PDE-III inhibitor) may be considered via Special Access Scheme.

Levosimendan

Typically given as a single 24-hour infusion. No active weaning required — the drug's prolonged active metabolite (OR-1896) tapers over 7–10 days. Haemodynamic effects diminish gradually. Re-dosing at 2–4 weekly intervals may be considered in advanced HF for palliation of symptoms.

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Bridge vs. destination: Inotrope-dependent patients who cannot be weaned should be urgently assessed for advanced HF therapies (cardiac transplant evaluation, LVAD, or palliative care pathway) at an Australian transplant centre (e.g., St Vincent's Sydney, Alfred Melbourne, Prince Charles Brisbane). Prolonged inotrope infusion without a clear destination plan is associated with poor outcomes.

Discharge Planning

Discharge planning begins on the day of admission and is a critical determinant of 30-day readmission — the key quality metric for ADHF care in Australia. The ACSQHC Clinical Standards for Heart Failure (2021) mandate structured discharge processes including medication reconciliation, patient education, and early follow-up.

Decongestion Endpoints Before Discharge

Patients should not be discharged until adequate decongestion is achieved. Residual congestion at discharge is the single strongest predictor of 30-day readmission. Clinical targets include:

Endpoint	Target	Assessment
Weight loss	≥ 0.5–1.0 kg/day during active diuresis	Daily weight (same time, same scale, same clothing)
Net fluid loss	≥ 1–1.5 L/day (or ≥ 100 mL/hr urine during diuresis)	Strict I&O chart; catheter removal once target reached
Orthopnoea	Resolution (can lie flat or ≤ 1 pillow)	Patient report
JVP	< 8 cm H₂O (not visible at 45°)	Clinical examination
Peripheral oedema	Trace or absent	Pitting oedema grading
NT-proBNP trajectory	≥ 30% reduction from admission level	Pre-discharge bloods (BNP/NT-proBNP)
Renal function	Stable or acceptable rise (up to 30% ↑ creatinine tolerated if congestion resolving)	UEC on day of discharge

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Do not discharge with residual congestion: Studies consistently show that patients discharged with > 1 kg above their estimated dry weight or with ongoing orthopnoea have 2–3× higher 30-day readmission rates. If diuretic targets are not met, continue inpatient treatment, reassess diuretic strategy, and consider adding metolazone or consultation for ultrafiltration.

Guideline-Directed Medical Therapy (GDMT) Optimisation

Every ADHF admission is an opportunity to initiate or uptitrate the four foundational pillars of HFrEF therapy. The "Start Low, Go Slow" approach applies during acute illness, but therapy should be started before discharge whenever feasible.

ACEi / ARB / ARNI

Sacubitril–valsartan (Entresto®) preferred if LVEF ≤ 40%

Start 24/26 mg BD; uptitrate to 97/103 mg BD

Washout 36 hrs from ACEi before starting ARNI. PBS Authority Required. K⁺ < 5.0, eGFR > 25.

Beta-blocker

Carvedilol (Dilatrend®) or bisoprolol or metoprolol succinate (CR/XL)

Start low once euvolaemic and stable (HR > 60, SBP > 90)

Do NOT initiate during acute decompensation with congestion. Resume at pre-admission dose if previously on BB.

MRA

Spironolactone (Aldactone®) or eplerenone (Inspra®)

Start 25 mg daily; uptitrate to 50 mg daily

K⁺ must be < 5.0 mmol/L and eGFR > 30. Monitor K⁺ at 3 days, 1 week, then monthly.

SGLT2 inhibitor

Dapagliflozin (Forxiga®) or empagliflozin (Jardiance®)

10 mg PO daily — initiate once euvolaemic, regardless of diabetes

DAPA-HF, EMPEROR-Reduced, EMPEROR-Preserved trials: mortality + HF hospitalisation benefit. PBS-listed for HFrEF (Authority Required). eGFR > 20.

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SGLT2 inhibitors — now standard of care: Per the 2024 NHF/CSANZ guidelines, SGLT2 inhibitors should be considered a foundational pillar alongside ACEi/ARBi, beta-blocker, and MRA in all patients with HFrEF (LVEF ≤ 40%). Initiate during the index admission once the patient is stabilised and euvolaemic. Dapagliflozin and empagliflozin are PBS-listed for HFrEF indication (Authority Required).

Additional Medications at Discharge

Oral diuretic: Transition IV furosemide to oral at 2× the IV dose (e.g. 40 mg IV → 80 mg PO). Some patients require 1:1 conversion with bumetanide. Discharge on a maintenance dose; patients may self-adjust (HF nurse-led titration) based on daily weight.
Iron replacement: If iron deficiency identified (ferritin < 100 or ferritin 100–299 with TSAT < 20%), IV iron (ferric carboxymaltose/Ferinject® 500–1000 mg IV single dose) improves symptoms and exercise capacity (AFFIRM-AHF, IRONMAN trials). PBS Authority Required for IV iron in HF.
Anticoagulation: If concurrent AF, ensure appropriate anticoagulation (DOAC preferred: apixaban, rivaroxaban, dabigatran, edoxaban). Assess CHA₂DS₂-VASc and HAS-BLED scores.
Vaccination: Ensure influenza (annual) and pneumococcal (Prevenar 13® + Pneumovax 23®) vaccination are up to date.

Early Follow-Up & Readmission Prevention

1

7-day post-discharge follow-up

Ideally with a HF specialist nurse or GP. Check weight, symptoms, UEC (diuretic safety), medication adherence. This is an ACSQHC Clinical Standard and NHF/CSANZ Class I recommendation. Telehealth is acceptable for remote/regional patients.

2

Multidisciplinary HF programme

Enrol in a structured HF management programme (in-person or telehealth). Australian programmes such as Heart Foundation MyHeart MyLife, state-based HF services, and cardiac rehabilitation reduce 30-day readmission by 25–35%.

3

Self-management education

Teach daily weight monitoring (same time, same scale), fluid restriction (1.5–2 L/day), low-sodium diet (< 2 g/day), recognition of decompensation signs (3 kg weight gain over 3 days, increasing dyspnoea, worsening oedema), and when to seek emergency care.

4

Medication reconciliation

Discharge medication list reviewed by pharmacist. Ensure patient understands each medication, dose, timing. Address cost barriers (PBS Safety Net, concession cards). Provide written medication plan in preferred language.

5

Cardiologist follow-up

Referral to a cardiologist or HF specialist within 4–6 weeks if not already under specialist care. Review echocardiography, GDMT titration trajectory, device candidacy (ICD/CRT), and advanced therapy assessment if recurrent admissions.

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Palliative care integration: For patients with advanced HF (NYHA IV, recurrent hospitalisations despite optimal therapy, inotrope-dependent, or declining advanced therapies), early integration of palliative care improves symptom burden and quality of life. The Australian Commission on Safety and Quality in Health Care recommends palliative care referral discussions for all patients with ≥ 3 HF hospitalisations in 12 months.

Special Populations

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Pregnancy

Peripartum cardiomyopathy: Presents in the last month of pregnancy or within 5 months postpartum. LVEF < 45% in the absence of other causes. Incidence in Australia ~1:1000 pregnancies.
ACEi/ARB/ARNI: Contraindicated in pregnancy (teratogenic — renal agenesis, oligohydramnios). Use hydralazine + nitrate combination as alternative vasodilator.
Beta-blockers: Labetalol or metoprolol preferred (relatively safe in pregnancy). Carvedilol — limited safety data; avoid if possible.
Diuretics: Furosemide — may reduce placental perfusion; use cautiously for fluid overload. Avoid thiazides (neonatal thrombocytopaenia risk).
MRA: Spironolactone — anti-androgenic effects in first trimester; contraindicated. Eplerenone — limited data; avoid.
SGLT2 inhibitors: Contraindicated in pregnancy and breastfeeding.
Delivery planning: Multidisciplinary team (obstetrics, cardiology, anaesthesia). Vaginal delivery preferred with epidural and passive second stage. C-section only for obstetric indications.

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Paediatrics

Aetiology: Congenital heart disease, myocarditis, dilated cardiomyopathy, and inborn errors of metabolism are the leading causes of paediatric HF in Australia.
Diuretics: Furosemide 0.5–1 mg/kg/dose IV q6–12h (max 6 mg/kg/day). Oral: 1–2 mg/kg BD. Monitor closely for dehydration and electrolyte disturbance.
ACEi: Enalapril 0.1 mg/kg PO BD (start low, titrate). Captopril 0.1–0.3 mg/kg PO TDS for neonates.
Beta-blockers: Carvedilol 0.05 mg/kg PO BD, uptitrate to 0.4 mg/kg BD. Limited paediatric evidence — use with specialist guidance.
BNP in children: Higher baseline values than adults. NT-proBNP > 300 pg/mL is suggestive in children; age-specific reference ranges apply.
Referral: All paediatric HF patients should be managed at a paediatric cardiac centre (e.g., Royal Children's Melbourne, Children's Hospital Westmead, Queensland Children's Hospital).

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Elderly (≥ 75 years)

HFpEF prevalence: Over 50% of HF admissions in those ≥ 75 years are HFpEF. Diagnostic criteria include typical symptoms, preserved LVEF, and evidence of diastolic dysfunction/raised filling pressures.
Diuretic caution: Increased risk of hypotension, falls, prerenal AKI, and electrolyte derangement. Start at lower doses and titrate slowly. Avoid over-diuresis (dry = hypotension + AKI).
Polypharmacy: Conduct a comprehensive medication review. Deprescribe nephrotoxic agents (NSAIDs), anticholinergics, and medications contributing to fluid retention. Involve a pharmacist.
Frailty assessment: Use validated tools (Clinical Frailty Scale). Frailty predicts mortality independent of HF severity and informs goals of care.
SGLT2 inhibitors: Effective in HFpEF (EMPEROR-Preserved, DELIVER trials). Well tolerated in the elderly — monitor for genital mycotic infections and volume depletion.

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Renal Impairment

Cardiorenal syndrome: Worsening renal function during ADHF treatment is common (up to 30%). A creatinine rise of up to 30% is acceptable if congestion is improving ("pseudo-worsening"). Avoid stopping diuretics prematurely.
Diuretics: Higher IV furosemide doses needed (up to 250 mg IV bolus). Continuous infusion may be more effective. Metolazone retains efficacy in severe CKD (unlike thiazides).
ACEi/ARB/ARNI: Continue if eGFR ≥ 25 and K⁺ < 5.5. May need dose reduction. Monitor UEC at 48 hrs after initiation or dose change.
MRA: Contraindicated if eGFR < 30 or K⁺ ≥ 5.0. Use lower doses (12.5–25 mg spironolactone). Monitor closely.
SGLT2 inhibitors: Can be initiated if eGFR ≥ 20 (per current PBS criteria). Benefits attenuate but do not disappear with declining GFR. Do not use for glycaemic control below eGFR 45; use for HF benefit regardless.
Dialysis: Refractory fluid overload with CKD may require haemodialysis or haemodiafiltration. Discuss with nephrology early.

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Hepatic Impairment

Congestive hepatopathy: Raised ALT/AST and bilirubin are common in ADHF from hepatic venous congestion. Differentiate from ischaemic hepatitis (acute ALT > 1000) which suggests severe low cardiac output.
Diuretics: Hepatomegaly and ascites may impair GI absorption of oral diuretics — use IV route. Monitor for hepatorenal physiology (Type 2 HRS) in severe right heart failure.
ACEi/ARB: Use with caution in severe hepatic impairment (Child-Pugh C). Metabolism of some agents is hepatic (e.g. losartan). No adjustment needed for most agents in mild-moderate impairment.
Anticoagulation: DOACs contraindicated in Child-Pugh C; warfarin with INR monitoring preferred. Apixaban may be used in Child-Pugh B with caution.

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Immunocompromised

Consider broader differentials: Myocarditis (viral, CMV, EBV, HIV), cardiac allograft rejection (post-transplant), drug-induced cardiotoxicity (anthracyclines, checkpoint inhibitors, trastuzumab), cardiac sarcoidosis.
Immunosuppression interactions: Cyclosporin and tacrolimus cause renal impairment and hypertension — interacts with diuretic and ACEi therapy. Corticosteroids cause fluid retention and hyperglycaemia.
Chemotherapy-related HF: If anthracycline-related cardiomyopathy suspected, initiate standard HF GDMT. ACEi/ARB + carvedilol may have cardioprotective role if initiated early (OVERCOME trial). Refer cardio-oncology.
Infection risk: Patients on high-dose diuretics or inotropes with indwelling catheters are at increased risk of line-related sepsis. Minimise line duration; aseptic technique for all central access.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health

Aboriginal and Torres Strait Islander Australians experience heart failure at 2–3 times the rate of non-Indigenous Australians, with significantly younger age at presentation, higher rates of HFrEF (often rheumatic heart disease-related in remote communities), and poorer outcomes including higher 30-day readmission and in-hospital mortality rates (AIHW, 2023). The burden is greatest in remote and very remote communities, where access to cardiology services, echocardiography, and cardiac rehabilitation is limited.

Disease burden

HF hospitalisation rates are 2.7× higher for Indigenous Australians. Rheumatic heart disease (RHD) remains a leading cause of HF in remote NT, WA, and QLD communities. Presentation is typically younger (median age 50s vs 70s non-Indigenous).

Remote access barriers

Many remote communities lack on-site echocardiography, specialist cardiology input, and HF nurse services. Telehealth cardiac clinics (e.g., NT Cardiac, RFDS) are critical but intermittent. Medication supply may be irregular in very remote areas; Pharmacy Remote Area Aboriginal Health Worker programmes are essential.

Cultural safety

Health literacy resources must be in culturally appropriate formats — use plain English, visual aids, and local language where possible. Involve Aboriginal and Torres Strait Islander health workers and liaison officers (AHLOs) in all HF education. "Sorry Business" and kinship obligations may affect follow-up adherence; flexibility in scheduling is essential.

RHD and HF

Secondary prophylaxis with benzathine penicillin G (BPG) 4-weekly IM is critical for RHD-related HF. Adherence to BPG is a major challenge — supported self-management and community-based delivery improve rates. Refer to RHDAustralia guidelines. Echocardiographic screening programmes are expanding under the END RHD strategy.

GDMT access

PBS medicines (ARNI, SGLT2i, MRA, beta-blockers) should be accessible under PBS co-payment with a valid Medicare card and concession status. Remote Area Aboriginal Health Services can supply medicines free of charge under Section 100 arrangements. Ensure medication continuity during patient transfer between community and hospital.

Cardiac rehabilitation

Participation in cardiac rehab is significantly lower for Indigenous Australians. Culturally adapted programmes (e.g., "Heart Health" programmes run by Aboriginal Community Controlled Health Organisations, ACHOs) show improved engagement. Exercise-based rehab and yarning circle models of education have shown promise in pilot programmes.

Social determinants

Overcrowded housing, food insecurity (limited access to fresh fruit and vegetables in remote communities), and high rates of comorbid diabetes, CKD, and smoking contribute to HF risk and complicate management. Multidisciplinary primary healthcare teams (GP, nurse, AHW, dietitian, social worker) are essential. Close the Gap PBS co-payment exemptions may apply.

Recommended actions

Screen for RHD in at-risk communities (Echo screening programmes). Refer to HF specialist (via telehealth if needed) early in admission. Ensure all GDMT is commenced and supplies arranged before discharge from urban hospitals back to remote communities. Arrange follow-up through local Aboriginal Medical Service (AMS) with HF care plan. Engage AHLO for discharge education and family involvement.

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Transfer of care: When Indigenous patients are repatriated to remote communities after an urban HF admission, ensure a warm handover to the receiving health service with a comprehensive HF management plan, medication supply for ≥ 4 weeks, and a confirmed follow-up appointment. Poor transfer-of-care processes contribute disproportionately to preventable readmissions in this population.

📚 References

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2. Australian Commission on Safety and Quality in Health Care (ACSQHC). Clinical Care Standards: Acute Heart Failure Clinical Care Standard. Sydney: ACSQHC; 2021.
3. Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2022;145(18):e895-e1032.
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8. McMurray JJV, Solomon SD, Inzucchi SE, et al. Dapagliflozin in patients with heart failure and reduced ejection fraction (DAPA-HF). N Engl J Med. 2019;381(21):1995-2008.
9. Packer M, Butler J, Filippatos GS, et al. Empagliflozin in patients with heart failure, reduced ejection fraction, and volume overload (EMPEROR-Reduced). N Engl J Med. 2020;383(15):1413-1424.
10. Anker SD, Butler J, Filippatos G, et al. Empagliflozin in heart failure with a preserved ejection fraction (EMPEROR-Preserved). N Engl J Med. 2021;385(16):1451-1461.
11. Vaduganathan M, Claggett BL, Jhund PS, et al. Estimating lifetime benefits of comprehensive disease-modifying pharmacological therapies in patients with heart failure with reduced ejection fraction: a comparative analysis of three randomised controlled trials. Lancet. 2024;403(10422):147-156.
12. Australian Institute of Health and Welfare (AIHW). Heart, stroke and vascular disease — Australian facts. AIHW; Canberra: 2023.
13. RHDAustralia (ARF/RHD writing group). The 2020 Australian guideline for prevention, diagnosis and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
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